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Updated: May 21, 2025

Competitive Transplants to Evaluate Hematopoietic Stem Cell Fitness
Published on: August 31, 2016
Kidney function after nonmyeloablative hematopoietic cell transplant for sickle cell disease
Emily Limerick1, Matthew M Hsieh1, Mauricio Barretto1
1National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Hematopoietic cell transplantation (HCT) is potentially curative for patients with sickle cell disease (SCD). Both SCD and HCT cause kidney damage. This study analyzed data from 160 patients who received nonmyelablative HCT for SCD. Renal function was assessed at baseline and annually for 3years. The rate of new-onset eGFR <60 ml/min/1.73m2 was low (2.8%). Rapid kidney function decline in the first year post-HCT was noted in 7.5% of patients but was not associated with subsequently worse renal function. The eGFR decreased post-HCT (1 year: -7.19 p < 0.0001, 2 year: -11.32 p < 0.0001, 3 year: -12.37 ml/min/1.73m2 p < 0.0001). Mean eGFR remained within normal limits throughout the follow-up period (1 year:119, 2 year:115, 3 year:113 ml/min/1.73m2). Hyperfiltration rates decreased with a corresponding increase in patients with normal eGFR post-HCT. Therefore, the decline in eGFR after HCT may represent preservation of renal function. The prevalence of kidney damage increased transiently but, by 3 years post-HCT, was not significantly changed from baseline. Most cases of kidney damage were due to albuminuria. AKI, noted early post-HCT in 39% of patients, was most commonly stage 1 and was associated with decreased survival (p = 0.03). Larger studies with longer follow-up are required to explore the effects of HCT on renal function in patients with SCD.
Hematopoietic cell transplantation (HCT) is potentially curative for patients with sickle cell disease (SCD). Both SCD and HCT cause kidney damage. This study analyzed data from 160 patients who received nonmyelablative HCT for SCD. Renal function was assessed at baseline and annually for 3years. The rate of new-onset eGFR <60 ml/min/1.73m2 was low (2.8%). Rapid kidney function decline in the first year post-HCT was noted in 7.5% of patients but was not associated with subsequently worse renal function. The eGFR decreased post-HCT (1 year: -7.19 p < 0.0001, 2 year: -11.32 p < 0.0001, 3 year: -12.37 ml/min/1.73m2 p < 0.0001). Mean eGFR remained within normal limits throughout the follow-up period (1 year:119, 2 year:115, 3 year:113 ml/min/1.73m2). Hyperfiltration rates decreased with a corresponding increase in patients with normal eGFR post-HCT. Therefore, the decline in eGFR after HCT may represent preservation of renal function. The prevalence of kidney damage increased transiently but, by 3 years post-HCT, was not significantly changed from baseline. Most cases of kidney damage were due to albuminuria. AKI, noted early post-HCT in 39% of patients, was most commonly stage 1 and was associated with decreased survival (p = 0.03). Larger studies with longer follow-up are required to explore the effects of HCT on renal function in patients with SCD.
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